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Cancer Cell. 2007 Aug;12(2):104-7.

A new mutational AKTivation in the PI3K pathway.

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1
Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.

Abstract

Although multiple members of the phosphatidylinositol-3-kinase pathway (PI3K) are targeted by germline or somatic mutations, functional mutations in the three akt isoforms have proven elusive. This is somewhat surprising, as AKT represents a key node in the PI3K pathway, exhibiting transforming activity when incorporated into the AKT8 retrovirus. A recent report in Nature identifies a transforming E17K PH domain mutation in akt1 in breast (8%), colorectal (6%), and ovarian (2%) cancers. E17K-akt1 transforming activity appears due to PtdIns(3,4)P2- and PtdIns(3,4,5)P3-independent recruitment of AKT1 to the membrane. This novel observation raises important theoretical and clinical questions.

PMID:
17692802
DOI:
10.1016/j.ccr.2007.07.014
[Indexed for MEDLINE]
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